The results provide evidence that the composite genotypes studied show interaction with smoking, the main exposition-related risk factor of periodontal disease. Non-smoking subjects are not at increased risk, even if they are genotype-positive.

Polymorphisms influencing the binding affinity between the Fcgamma receptors and IgG of different subclasses are thought to be of importance in the individual susceptibility to infections with Gram-negative bacteria contributing to periodontal disease. One hundred and fifty-four Caucasian subjects were clinically and radiographically examined for their periodontal status and genotyped for their allelic pattern of FcgammaRIIa, FcgammaRIIIa, and FcgammaIIIb polymorphism. In assessing periodontitis according to mean probing depth and attachment loss, no differences were found in allele frequencies or combined allotypes between the subjects with mild or moderate and those with severe signs of periodontitis. However, the extent and severity of bone loss were significantly associated with the genotype of the receptor FcgammaRIIIa. An increased risk of severe bone destruction was observed in individuals carrying the FcgammaRIIIa-VV genotype (OR = 5.3; 95% CI 1.4-26.2). FcgammaRIIIb is in linkage disequilibrium with FcgammaRIIIa. Hence it is also related to periodontal disease. There is no indication of an association between the polymorphism of FcgammaRIIa and periodontitis. The results are evidence that the FcgammaRIIIa genotype coding for the high affinity receptor imposes an additional risk of bone loss as does the FcgammaRIIIb genotype coding for the low affinity receptor.

The data suggest that the slow acetylator phenotype may be associated with a higher risk of periodontitis, especially in smokers. Possible explanations regarding the mechanism are discussed; however, such attempts are highly speculative at this time.

Periodontal disease is a common multifactorial process that leads to bone destruction and tooth loss. Interactions of environmental and genetic factors determine the extent and severity of periodontal disease. Smoking is one of the risk factors for periodontal disease, and the risk may be influenced by the polymorphism of N-acetyltransferase (NAT2) via metabolism of smoke-derived xenobiotics. We therefore hypothesized that a NAT2 genotype would be a risk factor for periodontal disease. A total of 154 Caucasian subjects were assigned to one of two groups (1) no or mild and (2) severe periodontal disease based on radiographic (bone destruction) and clinical criteria (probing depth, attachment loss) and the number of teeth. In all subjects genotyping for mutations on NAT2 was performed by means of PCR and RFLP analysis. In the less-affected group genotyping showed a fraction of predicted slow and rapid acetylators (53.6% and 46.4%, respectively) corresponding to the normal distribution in Caucasians. Severely affected patients were predominantly slow acetylators, the odds ratios being between 2.38 and 5.02 for the NAT2-related risk depending on the outcome parameters chosen. Adjustment for age had no influence on these findings. Our data indicate that the slow acetylator phenotype is associated with a higher risk of periodontitis, especially with respect to the severity of the disease. Possible implications with respect to the risk associated with smoking are discussed.

This investigation demonstrated that a dentifrice containing triclosan in combination with a copolymer can reduce plaque and gingival inflammation to levels comparable to regular interdental cleaning.